BackgroundThe independent prognostic impact of diabetes mellitus (DM) and prediabetes mellitus (pre‐DM) on survival outcomes in patients with chronic heart failure has been investigated in observational registries and randomized, clinical trials, but the results have been often inconclusive or conflicting. We examined the independent prognostic impact of DM and pre‐DM on survival outcomes in the GISSI‐HF (Gruppo Italiano per lo Studio della Sopravvivenza nella Insufficienza Cardiaca‐Heart Failure) trial.Methods and ResultsWe assessed the risk of all‐cause death and the composite of all‐cause death or cardiovascular hospitalization over a median follow‐up period of 3.9 years among the 6935 chronic heart failure participants of the GISSI‐HF trial, who were stratified by presence of DM (n=2852), pre‐DM (n=2013), and non‐DM (n=2070) at baseline. Compared with non‐DM patients, those with DM had remarkably higher incidence rates of all‐cause death (34.5% versus 24.6%) and the composite end point (63.6% versus 54.7%). Conversely, both event rates were similar between non‐DM patients and those with pre‐DM. Cox regression analysis showed that DM, but not pre‐DM, was associated with an increased risk of all‐cause death (adjusted hazard ratio, 1.43; 95% CI, 1.28–1.60) and of the composite end point (adjusted hazard ratio, 1.23; 95% CI, 1.13–1.32), independently of established risk factors. In the DM subgroup, higher hemoglobin A1c was also independently associated with increased risk of both study outcomes (all‐cause death: adjusted hazard ratio, 1.21; 95% CI, 1.02–1.43; and composite end point: adjusted hazard ratio, 1.14; 95% CI, 1.01–1.29, respectively).ConclusionsPresence of DM was independently associated with poor long‐term survival outcomes in patients with chronic heart failure.Clinical Trial Registration
URL: http://www.clinicaltrials.gov. Unique identifier: NCT00336336.
Cellular 'phones may be dangerous for pacemaker patients. However, they can be used safely if patients do not carry the 'phone close to the pacemaker, which is the only place where high risk interference has been observed.
External defibrillation is widely used for the termination of various atrial and ventricular tachyarrhythmias, including pacemaker patients. Our study was intended to evaluate the effects of DC shocks in 36 patients with unipolar pacemakers implanted in the right pectoral region (25 DDD, 10 VVI, 3 AAI). The shocks were delivered with paddles on the anterior surface of the thorax, as far as possible away from the pacemaker. The pacing output was programmed at 0.5 msec and 5 V (25 patients), 4 V (1 patient), and 2.5 V (10 patients). Transient loss of capture occurred in 18 patients (50%). These patients, compared with those without capture failure, received higher peak and cumulative shock energies, respectively, 216 +/- 99 versus 123 +/- 50 joules (P < 0.002) and 352 +/- 62 versus 147 +/- 98 joules (P < 0.004) and had a lower pacemaker pulse amplitude (4.0 +/- 1.2 vs 4.6 +/- 1.0 V, P = 0.11). Failure to capture lasted from 5 seconds to 30 minutes (mean 157 sec). In 15 patients the ventricular stimulation threshold was measured before and serially after cardioversion. A six-fold threshold increase was observed 3 minutes after the shock (P < 0.004) with gradual recovery to nearly baseline values at 24 hours. Transient sensing failure occurred in 7 of the 17 patients in whom it could be evaluated (41%). Furthermore, three cases of shock induced pacemaker malfunctions were observed requiring replacement of the stimulator in two patients. In conclusion, the incidence of loss of capture in pacemaker patients subjected to electrical cardioversion/defibrillation is high.(ABSTRACT TRUNCATED AT 250 WORDS)
Idiopathic VT of the LVOT can be treated successfully with RF ablation. ICE can accurately guide catheter ablation and identify anatomic landmarks, endocardial contact, and ablation electrode movement.
During spontaneous chronic AF in humans, (1) local capture by atrial pacing is possible up to at least 15 mm from the pacing site, (2) regional entrainment is possible during type 1 and type 2 AF but not type 3 AF, and (3) pacing before capture accelerates AF, probably by transient or local capture. These findings suggest that an excitable gap is present in chronic AF, therefore supporting the hypothesis that leading circle reentry is not the unique electrophysiological mechanism maintaining the arrhythmia.
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